An important model for preventing or treating the clinical symptoms of schizophrenia is derived from the NMDA glutamate receptor hypofunction (NRH) hypothesis. the circuitry proposed for the NRH hypothesis is based on evidence that specific receptor agonists and antagonists can block the neuropathologic impact of NRH on cortical neurons. Previous experiments demonstrating treatments that block NRH-induced neuropathologic changes provide a rationale for testing efficiacy of those treatments in blocking the clinical manifestations of NRH induced by the NMDA glutamate receptor antagonist, ketamine.